**7. Neuroanatomical and neuropsychological impairments in Capgras syndrome**

In 1971 a case of Capgras was described in a young man following a head injury, with no previous history of psychiatric disorder. Since then, many patients with CS have undergone more thorough neurological investigations [29]. Identification disorders like CS are very frequent in neurodegenerative diseases [7]. Regarding the organic conditions that occur in Capgras delusion, this appears mainly in various types of dementia like Alzheimer, Lewy bodies, and Parkinson [39]. The prevalence of CS in Lewy body dementia may be as high as 25% and 10% in Alzheimer-type dementia. Identification disorders are much rarer in other types of dementia, especially those associated with Parkinson's disease [7]. Nearly half of the cases in CS were associated with neurocognitive disorders, such as delirium, traumatic brain encephalopathy, cerebrovascular disease, dementia, meningioma, encephalitis, and multiple sclerosis [21, 22]. Although there is usually a delay in the presentation of Capgras delusion after cerebral events, there are also such cases of immediate presentation [31]. Psychotic disorders with CS tend to present in the late teens and early twenties. It reflects the long mean duration of the delusion in the functional group [26]. Those with neurological disorder associated with the onset of the delusion had a mean age of 60, in keeping with their presentation in middle to late adulthood, especially as Capgras delusion in dementia tends to occur in the later stages [26]. Therefore all individuals with Capgras should be examined for organic pathology [9]. In a literature review of patients with CS who had associated organic factors, there are several single case reports in patients with Capgras delusion which

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disorder [40].

condition's development [15, 17, 28].

*What is Capgras Syndrome? Diagnosis and Treatment Approach*

**8. Neuropsychological assessment for Capgras syndrome**

The term CS does not demonstrate a well-defined mental disorder. Over the years various studies have suggested psychodynamic and neurophysiological interpretations for CS, and various aetiologies have been recommended for the

Although frequently seen in psychotic cases, Capgras has also been associated with neurological disorders suggesting that the syndrome has an organic basis [14]. According to a study, CS patients were classified into groups according to whether or not they had evidence of neurological disorder. Some of the patients identified as having no neurological lesion might be found to have organic brain disease with more sophisticated imaging techniques or at post-mortem evaluation [41]. In another study, approximately one in five of patients with CS presented with organic mental disorders [1, 2]. Multiple hypotheses have been put forth regarding the underlying pathophysiology of CS. Some areas of the brain are responsible for the etiology of this disease. Results of structural and neuroimaging studies of CS provide support for an organic etiology [17]. Multiple studies and reports have remarked on CS in the setting of various neurological and neurodegenerative diseases [42]. There is a study that found more widespread bilateral frontal and temporal cortex atrophy in schizophrenia patients with CS than schizophrenia patients without the syndrome by using computerized tomography (CT) [17]. Likewise other studies using CT found global brain atrophy in combination with right hemisphere lesions in patients with dementia. There is also reported that positron emission tomography [PET] demonstrated

suggest structural and metabolic anomalies in mostly right-sided frontal, temporal, or parietal brain regions. But most of CS patients had bilateral lesions although, for those with unilateral lesions, right hemisphere lesions were much more likely [30]. Some studies give emphasis to the presence of two lesion sites, one in right frontal and the other in right temporal cortex [30]. The identity of the imposter is significantly associated with the reported underlying etiology. Capgras' delusion is reportedly due to functional psychiatric disorder, which is more likely to view their parent as an imposter, whereas the spouse is involved in those with suspected neurological etiology. There may be mentioned two reasons. The first one is may be because of the different mean age for the groups. The age of onset of Capgras delusion is different between those with organic disorders and those with neurological disorders [26]. The other reason is about Capgras delusion's feature. Capgras delusion is the phenomenon mostly specific to close relatives. This supports the role of intimacy [9, 26]. Selectivity for familiar persons is essential, though sometimes relative, and the syndrome can extend to persons who are simply known or famous [7]. Against this, the frequency with which strangers and multiple imposters are implicated in all cases of Capgras delusion can be up to 39% [26]. Multiple imposters are significantly more likely to occur in functional cases, while the involvement of inanimate objects would seem to suggest organic etiology [26]. The neuropsychological findings discussed may lead to some account of the possible mechanisms by which an abnormal experience may be generated in a subset of Capgras patients, but some researchers do not think in itself account for the formation of delusional belief [40]. Consequently, the explanation may offer a useful, helpful analysis of a certain step in the pathology of the CS in a subgroup of more neurological patients but could be unlikely to enlighten about delusions more generally or those with Capgras in the context of a functional psychosis such as schizophrenia or bipolar

*DOI: http://dx.doi.org/10.5772/intechopen.91153*

#### *What is Capgras Syndrome? Diagnosis and Treatment Approach DOI: http://dx.doi.org/10.5772/intechopen.91153*

*Anxiety Disorders - The New Achievements*

dominance of the lesions [32].

**syndrome**

**impairment, and confabulation**

**6. Cognitive domains in Capgras delusion: memory, executive** 

Neuropsychological deficits in patient with CS were reported across multiple cognitive domains, including memory, executive functioning, and visuospatial processing. These studies suggest that memory was statistically more likely to be impaired than other cognitive domains. Therefore, the memory may be playing an important role in the development of these delusions [32]. The existence of confabulations may have a role in prognosis and predicted significantly longer delusion duration, once more supporting the importance of memory impairment in patients with CS [32]. To mention a little more about the confabulation, some authors are focusing on confabulation in these patients because they are thought to be confabulation and delusion are closely related. When asked how they can explain their beliefs, Capgras patients will often confabulate. Confabulation is a kind of false memory that occurs when patients produce stories that fill in gaps in their memories, whereas a delusion is a mental state, typically thought of as a belief. Confabulation and delusion cannot be completely the same [37, 38]. Some researchers suggested that CS comes out when right hemisphere dysfunction causes a memory disconnection that leads to a failure to put new information together with representations about a significant individual and to keep in reserved over time [17]. Against all of these, although many patients have subtle deficits in face recognition and memory for faces, they do not have difficulty in recognizing faces in everyday life [1, 2]. CS is distinguished by its delusional mechanism: it is neither a hallucination nor an illusion—the object is correctly recognized in its appearance. CS is not a memory disorder. The person is correctly recognized; people are memorized [7]. Language deficits may not be absent, because of the right hemispherical

**7. Neuroanatomical and neuropsychological impairments in Capgras** 

In 1971 a case of Capgras was described in a young man following a head injury, with no previous history of psychiatric disorder. Since then, many patients with CS have undergone more thorough neurological investigations [29]. Identification disorders like CS are very frequent in neurodegenerative diseases [7]. Regarding the organic conditions that occur in Capgras delusion, this appears mainly in various types of dementia like Alzheimer, Lewy bodies, and Parkinson [39]. The prevalence of CS in Lewy body dementia may be as high as 25% and 10% in Alzheimer-type dementia. Identification disorders are much rarer in other types of dementia, especially those associated with Parkinson's disease [7]. Nearly half of the cases in CS were associated with neurocognitive disorders, such as delirium, traumatic brain encephalopathy, cerebrovascular disease, dementia, meningioma, encephalitis, and multiple sclerosis [21, 22]. Although there is usually a delay in the presentation of Capgras delusion after cerebral events, there are also such cases of immediate presentation [31]. Psychotic disorders with CS tend to present in the late teens and early twenties. It reflects the long mean duration of the delusion in the functional group [26]. Those with neurological disorder associated with the onset of the delusion had a mean age of 60, in keeping with their presentation in middle to late adulthood, especially as Capgras delusion in dementia tends to occur in the later stages [26]. Therefore all individuals with Capgras should be examined for organic pathology [9]. In a literature review of patients with CS who had associated organic factors, there are several single case reports in patients with Capgras delusion which

**124**

suggest structural and metabolic anomalies in mostly right-sided frontal, temporal, or parietal brain regions. But most of CS patients had bilateral lesions although, for those with unilateral lesions, right hemisphere lesions were much more likely [30]. Some studies give emphasis to the presence of two lesion sites, one in right frontal and the other in right temporal cortex [30]. The identity of the imposter is significantly associated with the reported underlying etiology. Capgras' delusion is reportedly due to functional psychiatric disorder, which is more likely to view their parent as an imposter, whereas the spouse is involved in those with suspected neurological etiology. There may be mentioned two reasons. The first one is may be because of the different mean age for the groups. The age of onset of Capgras delusion is different between those with organic disorders and those with neurological disorders [26]. The other reason is about Capgras delusion's feature. Capgras delusion is the phenomenon mostly specific to close relatives. This supports the role of intimacy [9, 26]. Selectivity for familiar persons is essential, though sometimes relative, and the syndrome can extend to persons who are simply known or famous [7]. Against this, the frequency with which strangers and multiple imposters are implicated in all cases of Capgras delusion can be up to 39% [26]. Multiple imposters are significantly more likely to occur in functional cases, while the involvement of inanimate objects would seem to suggest organic etiology [26]. The neuropsychological findings discussed may lead to some account of the possible mechanisms by which an abnormal experience may be generated in a subset of Capgras patients, but some researchers do not think in itself account for the formation of delusional belief [40]. Consequently, the explanation may offer a useful, helpful analysis of a certain step in the pathology of the CS in a subgroup of more neurological patients but could be unlikely to enlighten about delusions more generally or those with Capgras in the context of a functional psychosis such as schizophrenia or bipolar disorder [40].
